Rationale: Cardiac fibroblasts are key effector cells in the pathogenesis of cardiac fibrosis.
Transforming growth factor (TGF)-β/Smad3 signaling is activated in the border zone of …

Background—Postinfarction cardiac repair is regulated through timely activation and
repression of inflammatory pathways, followed by transition to fibrous tissue deposition and …

Background: Transforming growth factor–βs regulate a wide range of cellular responses by
activating Smad-dependent and Smad-independent cascades. In the infarcted heart, Smad3 …

TGF-βs regulate fibroblast responses, by activating Smad2 or Smad3 signaling, or via Smad-
independent pathways. We have previously demonstrated that myofibroblast-specific …

Repair of the infarcted heart requires TGF-β/Smad3 signaling in cardiac myofibroblasts.
However, TGF-β–driven myofibroblast activation needs to be tightly regulated in order to …

Rationale: TGF (transforming growth factor)-β is critically involved in myocardial injury,
repair, and fibrosis, activating both Smad (small mothers against decapentaplegic) …

We examined the role of the transforming growth factor (TGF)-β1 signaling inhibitor Smad 7
in cardiac fibrosis. TGF-β1 (10 ng/ml) was found to increase cytosolic Smad 7 expression in …

The master cytokine TGF-β mediates tissue fibrosis associated with inflammation and tissue
injury. TGF-β induces fibroblast activation and differentiation into myofibroblasts that secrete …

Most myocardial pathologic conditions are associated with cardiac fibrosis, the expansion of
the cardiac interstitium through deposition of extracellular matrix (ECM) proteins. Although …

Transforming growth factor-β1 (TGF-β1) signal and downstream Smads play an important
role in tissue fibrosis and matrix remodeling in various etiologies of heart failure. Inhibitory …